3. Functions of Bile Contains bile acids for fat digestion and absorption Emulsification of fat Aids in absorption of digested fat For excretion of wastes from the blood Bilirubin Excess cholesterol
4. Bile Flow Hepatocyte BileCanaliculi Perilobularductules Lobar ducts R & L hepatic ducts Common hepatic duct Common bile duct Gall bladder Cystic duct
8. Gallstone formation Too much water extraction from the bile Too much bile salt extraction from the bile Inflammation of the gallbladder wall Stasis
9. Regulation of Bile Flow Presence of bile acids More bile acids = more bile production Prevention of atherosclerosis Secretin Affects 2nd stage of bile production
10. Entero-Hepatic Circulation Liver Cholesterol Cholic Acid + Chenodeoxycholic Acid Conjugation with glycine or taurine Glyco- or Tauro- bile acids + NaCl Bile Salts Ileum SMV PV
11. Gallbladder pear-shaped sac 7 to 10 cm long average capacity of 30 to 50 mL When obstructed up to 300 ml Shared lymph and vascular drainage with liver
16. Triangle of Calot the area bound by the: cystic duct common hepatic duct liver margin
17. Cystic artery usually a branch of the right hepatic artery (>90% of the time) course of the cystic artery may vary, but it nearly always is found within the hepatocystic triangle it divides into anterior and posterior divisions
18. Cystic Artery Anomalies Most variable structure 90% from RIGHT hepatic artery 88% single, 12% double
19. Gallbladder mucus secreted into the gallbladder originates in the tubuloalveolar glands found in the mucosa lining the infundibulumand neckof the gallbladder, but are absent from the body and fundus histologically differs from the rest of the gastrointestinal tract i.e. lacks a muscularis mucosa and submucosa
22. PHYSIOLOGY During fasting cyclic emptying Amount of bile produced GB reabsorbs 90% of bile water Bile lithogenicity Cholesterol, phospholipids, bile salts Post-prandial Bile ejection GB, canaliculi CCK stimulants vs. inhibitors Extrahepatic bile duct no smooth muscle
41. Cholesterol Gallstones Unifying hypothesis Risk factors Age > 40 years old Female Race First degree relatives with gallstones Obesity Crohn’s disease Rapid weight loss Stasis Exogenous estrogen
51. CLINICAL SYNDROMES 2. Acute cholecystitis Complications Empyema of the gallbladder Emphysematous gallbladder Perforation, sepsis
52. CLINICAL SYNDROMES 2. Acute cholecystitis Complications Empyema of the gallbladder Emphysematous gallbladder Perforation, sepsis
53. CLINICAL SYNDROMES 2. Acute cholecystitis Treatment Avoid morphine and opioid analgesics Cholecystectomy Early vs. Late cholecystectomy Open vs. Lap Chole
64. CLINICAL SYNDROMES 7. Acalculouscholecystitis Ischemia Critically ill, fasting, septic patient, ICU Higher gangrene, empyema, perforation than in AC Cholecystectomy vs. cholecystostomy
65. CLINICAL SYNDROMES 8. Oriental Cholangiohepatitis Intrahepatic, extrahepatic BD with pigment stones Normal GB Hongkong Parasites in BD Ascarislumbricoides, Clonorchissinensis Segmental, hence, rare jaundice CBD exploration, biliary bypass
66. CLINICAL SYNDROMES 9. Cholecystitis and Biliary Colic in Pregnancy Ultrasound Historically, operate during 2nd trimester Currently, anytime during pregnancy Adequate tocolysis Open vs. laparoscopic cholecystectomy in pregnancy
67. CLINICAL SYNDROMES 10. Mirizzi Syndrome Type I- external CHD compression Cholecystectomy Type II- GB-CHD fistula Partial chole + biliary-enteric anastomosis Long cystic duct Painless jaundice, Cholangitis
69. Medical Treatment Oral dissolution therapy Urso- vs. chenodeoxycholic acid for 6-12 months For small, non-calcified cholesterol stones 50-60% response if <1cm 50% recur in 5 years
70. Medical Treatment Contact dissolution therapy MTBE directly to GB Mono-octanoin directly to CBD Dissolves in hours or days
71. Medical Treatment ESWL Criteria: biliary colic, <3 stones, functioning GB 12-18 months therapy= 91% clearance Experimental (2002) Complications Colic (20-40%), hemobilia (8-14%), mild AP (1-2%) Recurrence 33% in 5 years 15% with symptoms
